Fatal poisoning with blue vitriol

Cases of fatal poisoning with cupric compounds are relatively rare in everyday life and are not covered much in forensic literature. A case was encountered of fatal poisoning with a blue vitriol solution introduced into the uterine cavity in order to interrupt a pregnancy. A 39-year-old woman brought to the hospital by ambulance complained of pain in the lumbar region and profuse bloody genital discharge, which had appeared 3 days earlier. She believed she was 2 months pregnant and denied artificial interruption of the pregnancy. Upon examination, her condition was grave: a weak pulse of 80; blood pressure 100/60. The abdomen was soft, the liver and spleen not enlarged. Pasternak symptom was negative. The uterus was soft, painless and enlarged to 9 weeks of pregnancy. The uterine cervix was clean, the orifice closed. Discharge was profuse and bloody. The diagnosis was that she was 9 weeks pregnant and had a missed criminal abortion. Scraping out the uterus and corresponding therapy to control bleeding were ineffective. An operation was performed--extirpation of the uterus. However, despite the steps taken, the bleeding did not stop, and the patient's condition continued to worsen. 10 hours after being admitted to the hospital, she died. During forensic investigation, diffused, violet-colored cadaverous spots were discovered. Extensive subcutaneous hemorrhage was detected around the areas of injection. The skin covering was edematous; when pressed with a finger, areas of depression remained. There was about 250 ml of watery blood in the abdominal cavity. Internal organs were anemic. There were multiple subpleural, subepicardial, subcapsular, intraorgan and intramuscular micro- and macro-punctate hemorrhages; bleeding into the mucosa of the gastrointestinal tract and urinary tracts; and cerebral and pulmonary edema. Forensic histological examination showed acute circulatory disturbance with perivascular and peridiapedetic hemorrhage; concentrations of aggregated and hemolyzed erythrocytes in the small vessels and capillaries; cerebral, pulmonary and stromatic edema. In the kidneys there was coaugmentation of renal glomeruli; epithelial necrosis of part of the coiled ducts; lower epithelium in places had pigment grains; primarily in openings of straight ducts there were pigment cylinders; extreme plethora of the surrounding area, and infiltration from annular cells and polynuclears. Forensic chemical analysis showed 12.8 mg of copper; 6.6 mg in the uterus and 5.6 mg in the kidneys. From data obtained it can be concluded that the patient died from cupric compound poisoning, complicated by interruption of the pregnancy and uterine hemolytic hemorrhage. It was later established that during the month before being admitted to the hospital the patient introduced a solution of blue vitriol into the uterine cavity to interrupt the pregnancy.     

Fatal poisoning with sodium chloride

This is an account of accidental fatal poisoning of a psychiatric patient following the use of a saline emetic for suspected chlorpromazine poisoning.     

Fatal seizures associated with trimipramine poisoning

The present report describes a witnessed, fatal attack of seizures. Very high levels of trimipramine were found in the blood collected at autopsy. The cause of death would most likely have been misinterpreted as a suicidal intoxication if the attack had not been witnessed. Conversely, if toxicologic examination had not been undertaken, the fatality would probably have been registered as epilepsia.     

Fatal outcome of poisoning with ethylene glycol

After an act of violence, a delinquent swallowed about 250 ml ethylene glycol (EG) - probably to commit suicide before being arrested. During an interrogation by the police he appeared to be inebriated. A blood sample taken at this time did not contain ethanol but 5.1 g/l EG, as revealed by the analytical results. Only after a second examination was he taken to an intensive care unit in a hospital in spite of signs of pronounced intoxication after 12 h at the first examination. The patient died 30 h after taking EG without being effectively treated. The correct diagnosis, initiated by information from the poison control center, was made too late. At autopsy, findings were indicative of stage II of EG poisoning with a body burden of still 40-60 g EG. The mean rate of degradation in the blood was approximately 0.15 g/l per hour.     

Fatal outcome of poisoning with the benzodiazepines flunitrazepam and diazepam

On a wintry day a 29-year-old woman was found dead beside her car showing head injuries and signs of hypothermia. Several empty packets of sedative and hypnotic drugs were lying inside the car. Toxicological analysis revealed the presence of flunitrazepam (heart blood of the left and right chamber 0.033 mg/L each), norflunitrazepam (left heart blood 0.029 mg/L, right heart blood 0.027 mg/L), 7-amino-flunitrazepam (left heart blood 0.090 mg/L, right heart blood 0.104 mg/L), diazepam (left heart blood 0.395 mg/L, right heart blood 0.386 mg/L), nordazepam (left heart blood 0.112 mg/L, right heart blood 0.115 mg/L) and temazepam (left heart blood 0.034 mg/L, right heart blood 0.033 mg/L). Neither alcohol nor other drugs were found. It was concluded that benzodiazepine intake led to a disturbance of consciousness. Whether the woman died in this situation due to the icy temperature as a result of hypothermia or whether she died or would have died solely due to benzodiazepine overdosage could not be clarified.     

Fatal poisoning in drug addicts in the Nordic countries.

The study includes medicolegally examined fatal poisonings among drug addicts in 1997 in the five Nordic countries: Denmark, Finland, Iceland, Norway and Sweden, and the results are compared to a similar investigation from 1991. A common definition of "drug addict" was applied by the participating countries.The highest death rate by poisoning in drug addicts was observed in Denmark, where it was 6.54 per 10(5)inhabitants, followed by Norway with 6.35, Sweden with 2.21, Finland with 1.63 and Iceland with 1.20 per 10(5)inhabitants. All countries showed a higher death rate in 1997 than in 1991. For all countries the distribution of deaths according to geographical regions showed a decreasing number of drug deaths in the metropolitan area and an increasing number in other cities. Heroin/morphine dominated as the cause of death and was responsible for about 90% of the cases in Norway. In Sweden and Denmark, however, heroin/morphine caused only about 70% of the fatal poisonings. About 30% of the fatal poisonings in Denmark and Sweden were caused by other group I drugs, in Denmark mainly methadone and in Sweden mainly propoxyphene. Apart from two cases in Sweden methadone deaths were not seen in the other Nordic countries. In Finland heroin/morphine deaths have increased from about 10% in 1991 to about 40% in 1997. Forty-four percent of the fatal poisonings in Finland were caused by other group I drugs, mainly codeine and propoxyphene. The two fatal poisonings in Iceland were caused by carbon monoxide. Only few deaths in this investigation were caused by amphetamine and cocaine. A widespread use of alcohol, cannabis and benzodiazepines, especially diazepam, was seen in all the countries.     

Fatal poisoning with alcohol and drugs in the Greater Amman County

A study of fatal poisoning due to alcohol and drugs was carried out, to examine the mortality resulting from alcohol and drugs in the Greater Amman County, Jordan. A retrospective review of all autopsy records and certified deaths issued by the Department of Forensic Medicine at Jordan University Hospital in the greater Amman county was undertaken. During the 18 years (1978-1996) 6109 postmortem cases were performed in our department. A total of 60 cases were identified and analyzed according to age, race, sex, manner of death of the victims along with blood alcohol concentration, the drug detected at autopsies, the scene circumstances, and the geographic location of the accident and death.     

Fatal brodifacoum rodenticide poisoning: autopsy and toxicologic findings.

This report details the pathologic and toxicologic findings in the case of a 15-year-old girl who deliberately and fatally ingested brodifacoum, a commonly used rodenticide. The mechanism of death, massive pulmonary hemorrhage, has not been previously reported. Brodifacoum was quantitated in liver, spleen, lung, brain, bile, vitreous humor, heart blood, and femoral blood using HPLC with fluorescence detection. The highest brodifacoum concentrations were detected in bile (4276 ng/mL) and femoral blood (3919 ng/mL). No brodifacoum was detected in brain or vitreous humor. A brodifacoum concentration of 50 ng/g was observed in frozen liver while formalin fixed liver exhibited a concentration of 820 ng/g. A very high blood:liver brodifacoum concentration ratio suggested acute poisoning but the historical and pathologic findings suggested a longer period of anticoagulation. Though most cases of brodifacoum poisoning in humans are non-fatal, this compound can be deadly because of its very long half-life. Forensic pathologists and toxicologists should suspect superwarfarin rodenticides when confronted with cases of unexplained bleeding. Anticoagulant poisoning can mimic fatal leukemia or infectious diseases such as bacterial sepsis, rickettsioses, plague, and leptospirosis. A thorough death scene investigation may provide clues that a person has ingested these substances.     

Fatal venlafaxine overdose with acinar zone 3 liver cell necrosis

We present a case of fatal venlafaxine overdose in a 34-year-old male with a history of depression and previous suicide attempts. He presented unwell, and his condition deteriorated with the development of rhabdomyocytolysis and renal failure. Although treatment was provided, this was unsuccessful, and he died within a day of his admission. A postmortem examination was performed, and the findings included an acinar zone 3 pattern of liver cell necrosis and a very high level of serum venlafaxine in the deceased. No other elevated drug levels were detected. From this case, it is clear that venlafaxine overdose was the primary cause of a fatal acinar zone 3 pattern of liver cell necrosis. As far as we are aware, this is the first reported case of fatal acinar zone 3 liver necrosis caused by venlafaxine overdose alone.     

Fatal poisoning in drug addicts in the Nordic countries in 2007

The frequency of medico-legally examined fatal poisonings in 2007 among drug addicts was investigated in five Nordic countries; Denmark, Finland, Iceland, Norway, and Sweden. The number of deaths, age, sex, place of death, main intoxicant, and other drugs present in blood samples were recorded to obtain national and comparable Nordic data, as well as data to compare with earlier studies in 2002, 1997, and 1991. Norway had the highest incidence of drug addict deaths by poisoning followed by Denmark, with 8.24 and 6.92 per 100,000 inhabitants, respectively. The death rates in Finland (4.02), Iceland (4.56), and Sweden (3.53) were about half that of Norway and Denmark. Compared with earlier studies, the death rates were unchanged in Denmark and Norway, but increased in Finland, Iceland, and Sweden. In all countries, fewer deaths (29-35%) were recorded in the capital area compared with earlier studies. Females accounted for 11-19% of the fatal poisonings. Iceland deviates with a more equal distribution between men and women (40%). Deaths from methadone overdoses increased in all Nordic countries, and methadone was the main intoxicant in Denmark in 2007, accounting for 51% of the poisonings. In Norway and Sweden, heroin/morphine was still the main intoxicant with a frequency of 68% and 48%, respectively. In Iceland, 3 deaths each were due to heroin/morphine and methadone, respectively. Finland differs from other Nordic countries in having a high number of poisonings caused by buprenorphine and very few caused by heroin/morphine. The total number of buprenorphine deaths in Finland doubled from 16 in 2002 to 32 in 2007, where it constituted 25% of deaths. The general toxicological screening program showed widespread multi-drug use in all countries. The median number of drugs per case varied from 3 to 5. The most frequently detected substances were heroin/morphine, methadone, buprenorphine, tramadol, amphetamine, cocaine, tetrahydrocannabinol, benzodiazepines and ethanol.     

Fatal accidental mixed poisoning of 3 men at the same time]

The case history presented reports on three 30- to 40-years-old men, who were found dead in a party like situation in the living room. The toxicological investigation proved alcohol and THC as well as therapeutic Flunitrazepam- and Pentobarbital levels and toxic 7- Amino-Flunitrazepam concentrations. The background of this surprising scene led up to the conclusion of an accidental death caused by a mixed intoxication.     

Fatal colchicine poisoning by accidental ingestion of meadow saffron-case report

A 62-year-old male died of colchicine poisoning after accidental ingestion of Colchicum autumnale (meadow saffron). He ate a salad of plant with green leaves regarded as wild garlic (Allium ursinum). A few hours later he developed symptoms of gastroenteritis and was admitted to hospital. In spite of gastric lavage, activated charcoal and supportive measures, multi-organ system failure developed over the next two days. Laboratory analysis showed highly elevated blood concentrations of hepatic enzymes, creatine kinase, lactate dehydrogenase and blood urea nitrogen, as well as leukocytopenia and thrombocytopenia. Mechanical ventilation, dopamine, noradrenaline, crystalloid solutions and fresh frozen plasma were applied but despite treatment the patient died five days after the ingestion. Post-mortem examination revealed hepatic centrilobular necrosis, nephrotoxic acute tubular necrosis, petechial bleeding in fatty tissue, blunt and shortened intestinal villi and cerebral toxic edema. Botanical identification of incriminated plant gave Colchicum autumnale which confirmed colchicine poisoning. Although the accidental ingestion of Colchicum autumnale is rare and to our knowledge only five such cases have been described in detail, this is the second fatal case in Croatia described in the last 3 years.     

Fatal poisoning due to ingestion of boiled oleander leaf extract

Nerium oleander is an ornamental evergreen shrub belonging to the family Apocynaceae. The Apocynaceae family includes the attractive evergreen shrub known as oleander. The cardiotoxic glycoside, oleandrin, is present in all portions of the common oleander plant. Oleander consumption can result in deadly situations accidentally or as a suicide attempt. After consuming kettle-boiled oleander leaf extract as part of a suicide attempt, an 80-year-old man was discovered comatose in his home and taken to our emergency room. The patient's heart rate was 30 beats per minute, and he had hypotension. Arterial blood gas analysis revealed remarkable metabolic acidosis and hyperkalemia (K: 7.7 mEq/L). An electrocardiogram showed a wide QRS wave, similar to a sine curve. The patient collapsed following cardiac arrest soon after hospital arrival. Veno-arterial extracorporeal membrane oxygenation was initiated; however, the patient eventually died. The serum level of oleandrin at hospital arrival, subsequently measured by LC–MS/MS, was found to be 33.4 ng/mL, far above the levels reported in previous fatal cases.     

Fatal carbon monoxide poisoning after the detonation of explosives in an underground mine: a case report.

An unusual death caused by carbon monoxide poisoning after the detonation of explosives in an underground mine was investigated by the Office of the Medical Investigator of the State of New Mexico. The 50-year-old miner had 18 years of mining experience but no documented safety training. He collapsed approximately 20 minutes after entering the mine and working at the bottom of the single vertical shaft. The tight confines of the mine shaft hindered rescue personnel from reaching him, and the body was not recovered until 2 days later. The autopsy showed severe coronary artery atherosclerosis with remote and resolving myocardial microinfarcts, as well as the characteristic pink lividity of carbon monoxide poisoning, which was confirmed by laboratory analysis. Detailed investigation of the scene revealed no sources of carbon monoxide other than the explosives. The case represents an uncommon cause of death in mining that may have been avoided through the use of proper safety procedures, and illustrates the importance of recognizing the many sources of carbon monoxide.     

Fatal angioedema associated with captopril.

A markedly hypertensive, 70-year-old, black man had been on captopril for 2 years when he rapidly developed obstructive angioedema. The initial sign of difficulty in understanding his speech progressed to severe laryngeal and glossal edema over a 3 1/2 h period. His airway became obstructed less than a minute after arrival at the emergency room. Oral intubation was unsuccessful, and a difficult tracheostomy was too late to save the patient. The death was reported to the medical examiner because of its sudden and unusual nature. The risk of angioedema while on angiotensin converting enzyme inhibitor therapy has been noted previously in the clinical literature. Because of the sudden onset and possible confusion with an allergic reaction, this entity is brought to the attention of the forensic medical community.